| Amplification of chromosomal segment 4q12 in non-small cell lung cancer. | lung, |
| Advances in personalized therapeutics in non-small cell lung cancer: 4q12 amplification, PDGFRA oncogene addiction and sunitinib sensitivity. | lung, |
| PDGFRA gene rearrangements are frequent genetic events in PDGFRA-amplified glioblastomas. | glioblastoma, |
| PDGFRA mutants behave as oncogenes in this subset of gliomas | glioma, |
| Activation of Rac1 by Src-dependent phosphorylation of Dock180(Y1811) mediates PDGFRalpha-stimulated glioma tumorigenesis in mice and humans. | glioma, |
| A distinct spectrum of mutations confers constitutive receptor activation and oncogenic activity to PDGFRalpha in childhood high-grade gliomas. | glioma, |
| KIT and PDGFRA mutations appear to be alternative and mutually exclusive oncogenic mechanisms in gastrointestinal stromal tumors | None |
| The Receptor, PDGF alpha (PDGFRA)is implicated in the pathogenesis of AML, and the mechanisms of cytogenetic progression and oncoprotein-driven function may be similar in AML expressing oncogenic forms of PDGFRA. | None |
| PDGFRalpha mutations have been identified as alternative oncogenic mechanism in gastrointestinal stromal tumors. | None |
| As a sensitive and specific marker of GIST, PDGFR-alpha oncogenic mutations are more likely seen in giant, CD-117-negative GISTs arising outside the gastrointestinal tract and have an unfavorable clinical course. | None |
| The high rate of c-Kit/PDGFRA coexpression suggests that both receptors are involved in oncogenicity in gastrointestinal stromal tumors | None |
| Cyclin-dependent kinase 7/9 inhibitor SNS-032 abrogates FIP1-like-1 platelet-derived growth factor receptor alpha and bcr-abl oncogene addiction in malignant hematologic cells. | None |
| Constitutive activation of oncogenic PDGFRalpha-mutant proteins occurring in GIST patients induces receptor mislocalisation and alters PDGFRalpha signalling characteristics. | None |
| The oncogenic FIP1L1-PDGFRalpha fusion protein displays skewed signaling properties compared to its wild-type PDGFRalpha counterpart. | None |
| We report a unique case of an SDH-deficient GIST case with an activating PDGFRA mutation. Oncogenic mutations in GIST are generally mutually exclusive; however documented exceptions exist which may have diagnostic and therapeutic implications. | None |
| The current study shows that SH3BP2 is expressed in primary tumors and cell lines from Gastrointestinal stromal tumors (GISTs) patients and that SH3BP2 silencing leads to a downregulation of oncogenic KIT and PDGFRA expression and an increase in apoptosis in imatinib-sensitive and imatinib-resistant GIST cells. | None |